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(Hypertension. 1997;29:606-612.)
© 1997 American Heart Association, Inc.

Articles

Pressure-Overload Deinduction of Human ₂ Na,K-ATPase Gene Expression in Transgenic Rats

Nelson Ruiz-Opazo; Xie Hou Xiang; Victoria L.M. Herrera

the Sections of Molecular Genetics and Cardiology (V.L.M.H.), Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston (Mass) University School of Medicine.

Correspondence to Victoria L.M. Herrera, MD, Cardiology, Whitaker Cardiovascular Institute, Evans Department of Medicine, Boston University School of Medicine, 80 E Concord St, Boston, MA 02118. E-mail vherrera@acs.bu.edu

The early and sustained deinduction of ₂ Na,K-ATPase gene expression in both cardiac left ventricle and aorta in various pressure-overload rat models and in hypertrophied human heart suggests a common transcriptional pressure response mechanism to pressure overload in both rats and humans. To test this hypothesis, we developed transgenic rat lines expressing the chloramphenicol acetyltransferase reporter gene regulated by the human ₂ Na,K-ATPase (-798 to +67) regulatory region, H₂-CAT. Analysis of two homozygous transgenic rat lines revealed (1) parallel tissue-specific regulation of the H₂-CAT transgene and rat ₂ Na,K-ATPase gene and (2) parallel load-induced deinduction of both cardiac and vascular (aortic) H₂-CAT transgene and rat ₂ Na,K-ATPase gene expression in a 3-day model of induced pressure overload. Cardiac H₂-CAT deinduction was detected at a systolic pressure greater than or equal to 150 mm Hg and correlated with the degree of systolic pressure elevation (r=.82, P<.0001). The data suggest a systolic pressure gradient–dependent coordinate pressure-overload transcriptional response mechanism in the heart and aorta, with one of its target genes being the ₂ Na,K-ATPase gene in both humans and rats.

Key Words: Na⁺,K⁺-transporting ATPase • rats, transgenic • transcription, genetic

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